Intestinal PPARγ signalling is required for sympathetic nervous system activation in response to caloric restriction.

Détails

Ressource 1Télécharger: srep36937.pdf (1465.40 [Ko])
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_4F2384AD45B8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Intestinal PPARγ signalling is required for sympathetic nervous system activation in response to caloric restriction.
Périodique
Scientific Reports
Auteur⸱e⸱s
Duszka K., Picard A., Ellero-Simatos S., Chen J., Defernez M., Paramalingam E., Pigram A., Vanoaica L., Canlet C., Parini P., Narbad A., Guillou H., Thorens B., Wahli W.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
6
Pages
36937
Langue
anglais
Résumé
Nuclear receptor PPARγ has been proven to affect metabolism in multiple tissues, and has received considerable attention for its involvement in colon cancer and inflammatory disease. However, its role in intestinal metabolism has been largely ignored. To investigate this potential aspect of PPARγ function, we submitted intestinal epithelium-specific PPARγ knockout mice (iePPARγKO) to a two-week period of 25% caloric restriction (CR), following which iePPARγKO mice retained more fat than their wild type littermates. In attempting to explain this discrepancy, we analysed the liver, skeletal muscle, intestinal lipid trafficking, and the microbiome, none of which appeared to contribute to the adiposity phenotype. Interestingly, under conditions of CR, iePPARγKO mice failed to activate their sympathetic nervous system (SNS) and increase CR-specific locomotor activity. These KO mice also manifested a defective control of their body temperature, which was overly reduced. Furthermore, the white adipose tissue of iePPARγKO CR mice showed lower levels of both hormone-sensitive lipase, and its phosphorylated form. This would result from impaired SNS signalling and possibly cause reduced lipolysis. We conclude that intestinal epithelium PPARγ plays an essential role in increasing SNS activity under CR conditions, thereby contributing to energy mobilization during metabolically stressful episodes.

Pubmed
Web of science
Open Access
Oui
Création de la notice
15/12/2016 9:05
Dernière modification de la notice
20/08/2019 14:04
Données d'usage